Download Acute Angle Closure Glaucoma

Acute Angle Closure Glaucoma
Dr Tamara Al-Talib
GP ST2
21st November 2013
Aims
 Definition
 Pathophysiology
 Epidemiology
 Presentation & Diagnosis
 DDx
 Management
 Follow-up
 Complications
 Prognosis
Definition
 Glaucoma: Several ocular diseases that ultimately result in increased
intraocular pressure (IOP) and decreased visual acuity.
 Acute angle-closure glaucoma (AACG) is an ocular emergency
 Defined as at least 2 of the following symptoms:
 ocular pain
 nausea/vomiting
 history of intermittent blurring of vision with halos
 and at least 3 of the following signs:
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IOP greater than 21 mm Hg
conjunctival injection
corneal epithelial edema
mid-dilated nonreactive pupil
and shallower chamber in the presence of occlusion.
Pathophysiology
 Aqueous humor is produced by the ciliary body in the
posterior chamber of the eye. It diffuses from the posterior
chamber, through the pupil, and into the anterior chamber.
From the anterior chamber, the fluid is drained into the
vascular system via the trabecular meshwork and Schlemm
canal contained within the angle.
 Several anatomic abnormalities lead to anterior chamber crowding and
predispose individuals to AACG.
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a narrow angle has the most devastating consequences
shallower anterior chambers
thinner ciliary bodies
a thinner iris
anteriorly situated thicker lens
and a shorter axial eye length.
 Precipitating factors
 Drugs (sympathomimetics, anticholinergics, antidepressants [SSRIs],
anticonvulsants, sulfonamides, cocaine, botulinum toxin
 dim light
 rapid correction of hyperglycemia.
 Case reports have identified AACG associated with carotid-cavernous
sinus fistula, trauma, prone surgical positioning, and giant cell arteritis
Epidemiology
Mortality/Morbidity
 Dependent on duration from onset to treatment, underlying ocular disease,
and ethnicity.
 The degree of IOP elevation has been shown to have less impact on future
visual acuity.
 Studies report that as many as two thirds of individuals with AACG had no
visual field loss.
Race
 AACG occurs in 1 of 1000 whites, about 1 in 100 Asians, and as many as 2-4 of
100 Eskimos.
Sex
 AACG predominately affects females because of their shallower anterior
chamber.
Age
 Elderly patients in their sixth and seventh decades of life are at greatest risk.
Presentation - History
 Periorbital pain-‟boring‟
 Associated with ipsilateral headache
 Visual deficits- blurry vision and describe the phenomenon of
"seeing halos around objects.“
 In a large percentage of patients, extraocular symptoms and
systemic manifestations are the chief complaint.
 Headache
 Nausea and/or vomiting
 abdominal pain
 Precipitating factors
Presentation - Examination
 Visual acuity, the external eye, visual fields, a fundoscopic examination,
pupils, ocular motility, and IOP.
 Slit-lamp evaluation: corneal edema, synechiae, irregular pupil shape or
function, or segmental iris atrophy.
 Patients complain of blurred vision, and testing reveals the ability only to
detect hand movements. They are unable to identify numbers and letters
on distance charts or near cards.
 Cornea and scleral injection and ciliary flush are present. The obviously
edematous and cloudy cornea obscures the fundoscopic examination.
 Increased IOP (normal limit, 10-20 mm Hg) and ischemia result in pain
on eye movement, a mid-dilated nonreactive pupil, and a firm globe.
Diagnosis
 Clinical presentation and a physical examination.
 No definitive laboratory or imaging studies are available.
 However, tonometry must be performed and must
demonstrate increased intraocular pressure (IOP).
„‟TIME SENSITIVE DIAGNOSIS!”
DDX
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Acute Orbital Compartment Syndrome
Conjunctivitis
Corneal Abrasion
Corneal Laceration
Corneal Ulceration and Ulcerative Keratitis
Endophthalmitis
Glaucoma, Malignant
Glaucoma, Neovascular
Herpes Zoster Ophthalmicus
Iritis and Uveitis
Orbital Infections
Periorbital Infections
Ultraviolet Keratitis
Vitreous Hemorrhage
Management: GOAL = reduce IOP
 Prehospital Care:
 Emergency !!
1. Suppressing
aqueous
comfort and reduce IOP.
It is alsohumor
believed that, while supine, the
production
lens falls away from the iris
decreasing pupillary block.
 Remain in the supine position as long as possible-may aid in
 Avoid eye patches, covers, or blindfolds - maintaining the
conditions that cause pupillary dilation
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2. Reversing
Hospital Care:
inflammation
3. Eliminating
pupillary block
 Medical management is the first step - decreases the duration of
elevated IOP and the potential for visual field loss.
Management – Initial Tx
Decrease IOP-decrease aqueous humor production and to
enhance opening of the angle
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Carbonic anhydrase inhibitors - Acetazolamide should be given as a
stat dose of 500 mg IV followed by 500 mg PO
Topical Beta-adrenergic blockers - (ie, carteolol, timolol)
Alpha-adrenergic agonists – (ie. apraclonidine, brimonodine) can
be added for a further decrease in IOP.
Decrease the inflammatory reaction and reduce optic nerve
damage.
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Topical Corticosteroids- (ie. Prednisolone ophthalmic), 1-2 doses
 Extraocular manifestations
 analgesics for pain
 antiemetics for nausea and vomiting-can drastically increase IOP
Management – Reassessment
 Ophthalmic agents, miotic- (Pilocarpine) opening of the angle
 Approx 1 hour after beginning treatment, administered every 15
minutes for 2 doses.
 In the initial attack, the elevated pressure in the anterior chamber
causes a pressure-induced ischemic paralysis of the iris. At this time,
pilocarpine would be ineffective. During the second evaluation, the
initial agents have decreased the elevated IOP and hopefully have
reduced the ischemic paralysis so pilocarpine becomes beneficial in
relieving pupillary block.
 Pilocarpine must be used with caution! -constricting the ciliary
muscle, increase the axial thickness of the lens and to induce
anterior lens movement. This could result in reducing the depth of
the anterior chamber and worsening the clinical situation in a
paradoxical reaction.
Management – Reassessment
 Hyperosmotics – (ie. PO glycerin, isosorbride –in
diabetics or IV mannitol)
 If the IOP is not reduced 30 minutes after the second
dose of pilocarpine
 reduce vitreous volume, which, in turn, decreases
IOP.
 !!osmotic diuresis-not for cardiovascular and renal
patients.
 Repeat doses may be necessary if no effect is seen
and if tolerated.
Management – Reassessment
 Corneal indentation (CI)
 used as a temporizing measure to reduce IOP until definitive treatment is available.
 Laser peripheral iridotomy (LPI)-DEFINITIVE Tx
 performed 24-48 hours after IOP is controlled
 LPI may be offered prophylactically to individuals anatomically
predisposed to AACG if identified before the first acute attack.
 Argon laser peripheral iridoplasty (ALPI)
 burns made in the peripheral iris resulting in iris contraction and
opening of the angle
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Anterior chamber paracentesis (ACP)
Follow up
 Patients remain on oral acetazolamide, pilocarpine, and beta-
blockers or alpha-agonists until definitive treatment.
 After laser peripheral iridotomy (LPI), 33% of patients
require topical medication to maintain lower IOP.
Complications
 Permanent decrease in visual acuity
 Repeat episode
 Malignant glaucoma
 Fellow eye attack
 Central retinal artery occlusion
 Central retinal vein occlusion
Prognosis
 With adequate treatment, most patients recover their lost
vision.
 In whites, IOP was controlled with LPI alone in 65-76%.
 Asians more often have medically refractory initial attacks
and require medications after LPI. They also have higher rates
of visual field loss and subsequent increases in IOP.
Thank you